When I spent the better part of a year researching the state of the salt science back in 1998—already a quarter century into the eat-less-salt recommendations—journal editors and public health administrators were remarkably candid about how flimsy the evidence was implicating salt as the cause of hypertension.

In fact, an editor for the Journal of the American Medical Association told me at the time that the authorities pushing the eat-less-salt message had made a commitment to salt education that goes way beyond the scientific facts.

While, back then, the evidence merely failed to demonstrate that salt was harmful, the evidence from studies published over the past two years actually suggests that restricting salt can increase our likelihood of dying prematurely. Put simply, the possibility has been raised that if we were to eat as little salt as the USDA and CDC recommend, we’d harm rather than help ourselves.

A Hypothesis Yet to Be Proved

Why have we been told that salt is so deadly? The advice has always sounded reasonable: Eat more salt, and your body retains water to maintain a stable concentration of sodium in your blood. This is why salty food tends to make us thirsty: We drink more; we retain water. The result can be a temporary increase in blood pressure, which will persist until our kidneys eliminate both salt and water.

The scientific question is whether this temporary phenomenon translates to chronic problems: If we eat too much salt for years, does it raise our blood pressure, cause hypertension, then strokes, and then kill us prematurely? It makes sense, but it’s only a hypothesis. The reason scientists do experiments is to find out if hypotheses are true.

In 1972, when the National Institutes of Health introduced the National High Blood Pressure Education Program to help prevent hypertension, no meaningful experiments had yet been done. The best research on the connection between salt and hypertension came from two pieces of evidence. One was the repeated observation that populations that ate little salt had virtually no hypertension. But they didn’t eat a lot of things—sugar, for instance—and any one of those could have been the causal factor. The second was a strain of “salt-sensitive” rats that reliably developed hypertension on a high-salt diet. The catch was that “high salt” to these rats was 50 times more than what the average American consumes.

Still, the program was founded to help prevent hypertension, and prevention programs require preventive measures to recommend. Eating less salt seemed to be the best option at the time, short of losing weight. Although researchers quietly acknowledged that the data were “inconclusive and contradictory” or “inconsistent and contradictory”—two quotes from cardiologist Jeremiah Stamler, MD, a leading proponent of the eat-less-salt campaign, in 1967 and 1983—publicly, the link between salt and blood pressure was upgraded from hypothesis to fact.

In the years since, the NIH has spent enormous sums on studies to test the hypothesis, and those have singularly failed to make the evidence more conclusive. Instead, organizations advocating salt restriction today—the USDA, the Institute of Medicine, the CDC, and the NIH—all essentially rely on the results from one 30-day trial: the 2001 DASH-Sodium study. It suggested that eating significantly less salt would modestly lower blood pressure; it said nothing about whether this would prevent heart disease or lengthen life.